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British Journal of Ophthalmology, 1984, 68, 890-891
Ocular side effects of disopyramide
J. FRUCHT',
FREIMANN,2 AND S. MERIN'
From the Departments of ' Ophthalmology and 2Cardiology, Hadassah University Hospital, Kiryat Hadassah,
Jerusalem, Israel
I.
SUMMARY A patient who suffered from severe decrease of accommodation and pupillary dilatation
following the systemic use of disopyramide is described. The ocular side effects when this drug is
used in large doses result from its anticholinergic action.
Disopyramide (4 di-isopropylamino-2 phenyl-2-(2pyridyl) butyramide phosphate) is currently used as
an antiarrhythmic drug. ' 2 Its pharmacological effect
on the heart is thought to be known.'-3 Disopyramide
slows the depolarisation rate of the action potential,
depresses phase 4, and prolongs the duration of repolansation.' With the widespread use of the drug
several adverse side effects have been described.4
Most were caused by its anticholinergic action and
included dry mouth, urinary retention,5 and acute
angle closure glaucoma.6 Disopyramide has been reported47 to cause blurred vision, but no explanation
of its mechanism or dose dependence was given.
We describe a patient who suffered from accommodation and pupillary paralysis as a result of treatment with a high dose of disopyramide for ventricular
arrhythmia. The ocular effect of high systemic doses
of the drug seems to be equivalent to the anticholinergic effect of topical mydriatics and cycloplegics.
tests were within the normal range. The patient had
no ocular symptoms.
On her second day in hospital the attacks of ventricular tachycardia no longer responded to the usual
antiarrhythmic drugs and the cardiologist decided to
treat her with high doses of disopyramide. The
patient's weight was 49 kg. A dose of 200 mg of
disopyramide was injected intravenously and 150 mg
six times a day was given orally. On the next day the
oral dose was raised to 300 mg six times a day. This
dose finally prevented the attacks of ventricular
tachycardia. On the day following the disopyramide
101
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AA
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A
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E 6-
Case report
in S-
A 16-year-old girl was referred to the Department of
Cardiology, Hadassah University Hospital, because
of recurrent ventricular tachycardia refractory to
treatment by the usual antiarrhythmic drugs
(lignocaine, quinidine, pronestyl (procainamide
hydrochloride), hydantoin (phenytoin), verapamil,
and ajmaline). The patient was healthy until the first
ventricular tachycardia one-and-a-half months
before the present admission to the hospital. General
medical investigations ruled out viral, collagen, and
autoimmune diseases. The blood count, sedimentation rate, tri-iodothyronine, thyroxine, thyroid
stimulating hormone, calcium, phosphate, and other
Correspondence to Dr J. Frucht.
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0
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O 1
2 3 4 56 7 8 9 E0 11 12 13
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ft
Fig. 1 Relationship between pupillary size (@=mm),
accommodation (A =dioptres), and days of treatment.
The two single arrows indicate beginning and end of
disopyramide treatment. The double arrow indicates time of
increase of the dose of quinidine to 3 - 2 glday.
890
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Ocularside effects of disopyramide
891
treatment the girl complained that she could not see
well enough to read, had blurred vision, and a dry
mouth. Her visual acuity was OD 6/6, OS 6/7*5+.
The pupils were dilated to 8 mm, and the light reflex
was poor. The anterior and posterior segments were
normal. Refraction showed OD+0-75 6/6 OS+1-00
6/6; near point of convergence 5 cm. In each eye the
amplitude of accommodation was 2*50-3*00dioptres.
The patient was orthophoric. When +1-00 dioptre
was added she could read from a distance of 40 cm.
She continued to complain that she could not see well
enough to read, had photophobia and a dry mouth.
The disopyramide treatment was abruptly stopped
on the seventh day, and treatment with quinidine
1*8 g/day was started. This very large dose finally
controlled successfully the ventricular tachycardia.
Fig. 1 shows the amplitude of accommodation and
the pupillary changes during the presence of the
symptoms and after stopping the treatment by
disopyramide. The patient had recovered from all
abnormal ocular signs and symptoms by the next
morning 20 hours after taking the last dose of
disopyramide.
cholinergic effect on the parasympathetic system
probably caused the drop of amplitude of accommodation to 2*5-3 dioptres and pupillary dilatation to
8 mm. This effect is very similar to the effect of
atropine given by drops. However, the recovery time
was much shorter-less than 20 hours after stopping
treatment with disopyramide.4 The recorded
amplitude of accommodation was 7 dioptres and a
day later 8/2 dioptres. This still reduced amplitude of
accommodation might be explained by the alternative use of quinidine which also has some
antocholinergic effect.'0 Given the next day in a
higher dose (3-2 g/day) this drug probably caused the
additional reduction in amplitude of accommodation
from 8*50 dioptres to 7 dioptres. No effect on pupillary muscles was recorded.
The arrhythmia was controlled in our patient by a
very large amount of disopyramide. The treatment
was stopped because of visual system complications.
However, in cases that are not controlled by other
antiarrhythmic drugs these complications can be
overcome by using additional plus glasses for reading.
Discussion
References
One drop of atropine 1% instilled into the conjunctival sac of a young adult may cause pupillary
dilatation to 8 mm and reduction in the amplitude of
accommodation from 12 to four dioptres,8 while
systemic administration has much less effect. However, 1 mg or 2 mg injected subcutaneously into a
person weighing 70 kg reduces the amplitude of
accommodation by 20% and by 30% respectively.9
A decrease of amplitude of accommodation,
enough to cause inability to read following systemic
administration of drugs with known anticholinergic
side effects in a young patient, is very unusual. It has
never been reported after therapeutic doses of
atropine.
In the present case the high dose of disopyramide
given was similar to the high doses given to patients
with stubborn and refractile arrhythmias.4 The anti-
1 Singh BN, Collett JT, Chew CYC. New perspectives in the
pharmacologic therapy of cardiac arrhythmias. Prog Cardiovasc
Dis 1980; 22: 243-301.
2 Zipes DP, Toup PJ. New antiarrhythmic agents: amiodarone
aprinidine, disopiramide, athmozin, mexilectine, tocanide,
rerapamile, Am J Cardiol 1978; 41: 1005-24.
3 Danilo LP, Rosen MR. Cardiac effects of disopyramide. Am
Heart J 1976; 92: 532-6.
4 Koch-Weser J. Disopyramide. N Engl J Med 1979; 300: 957-62.
5 Large SH, Todd CH. Disopyramide associated with urinary
retention. Lancet 1977; ii: 1362.
6 Trope GE, Hind VMD. Closed-angle glaucoma in patient on
disopyramide. Lancet 1978; i: 329.
7 Braunwald E. Heart disease. A textbook of cardiovascular medicine. Philadelphia: Saunders, 1980; 713-4.
8 Wolf AV, Hodge HC. Effects of atropine sulfate, methylatropine nitrate (metropine) and hematropic hydrobromide on adult
human eyes. Arch Ophthalmol 1946; 36: 293-301.
9 Riker WF Jr. Contributions to medicine by research in pharmacology. JAMA 1962; 179: 355-60.
10 Braunwald E. Heart disease. A textbook of cardiovascular medicine. Philadelphia: Saunders, 1980; 707.
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Ocular side effects of disopyramide.
J Frucht, I Freimann and S Merin
Br J Ophthalmol 1984 68: 890-891
doi: 10.1136/bjo.68.12.890
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